中华医学杂志(英文版)
中華醫學雜誌(英文版)
중화의학잡지(영문판)
CHINESE MEDICAL JOURNAL
2002年
9期
1316-1320
,共5页
胡波%孙圣刚%梅光武%陈良怡%童萼塘
鬍波%孫聖剛%梅光武%陳良怡%童萼塘
호파%손골강%매광무%진량이%동악당
银杏叶提取物%自由基%兴奋/抑制性氨基酸%细胞内游离钙%缺血/再灌注
銀杏葉提取物%自由基%興奮/抑製性氨基痠%細胞內遊離鈣%缺血/再灌註
은행협제취물%자유기%흥강/억제성안기산%세포내유리개%결혈/재관주
ginkgo biloba extract%free radicals%excitatory aminoacids%inhibitory aminoacids%free intracellular calcium%cortex%hippocampus%ischemia%reperfusion
目的研究银杏叶提取物(GBE)对大鼠缺血再灌注损伤皮质内自由基、氨基酸动态平衡的影响及其对原代培养的大鼠海马神经元内游离钙离子浓度([Ca2+]i)的影响和特征.方法采用的动物模型参照Zivin JV 的大脑中动脉线栓模型以获得缺血/再灌注损伤的皮质组织样本.采用高压液相色谱仪测量氨基酸的浓度;MDA和GSH-PX采用TBA法测量,SOD采用嘌呤法测量.使用显微荧光检测系统检测单个原代培养的海马神经元内游离钙离子浓度([Ca2+]i)的变化和特征.结果和对照组比较,治疗组中,SOD和GSH-PX 的浓度较高, MDA的浓度则明显降低, 谷氨酸、天门冬氨酸的浓度明显降低,而GABA的浓度在各个时间点均升高(P<0.01), Gly的浓度在一些时间点有所降低 (P<0.05), 5 mg/kg 组与10 mg/kg、15 mg/kg组间有显著差别,而后二者间差别无显著意义.当向原代培养的神经元同时给予1×10-5 mol/L谷氨酸和25 μg/mlGBE20秒时所诱导的[Ca2+]i明显低于单独使用1×10-5 mol/L谷氨酸所引起的[Ca2+]I的变化,其峰值明显下降,且Phase 1上升速度减慢,Phase 2的时间也有所缩短,二相之间的平台期相对延长,当其返回基线后,再次给予1×10-5 mol/L谷氨酸时,其反应可恢复.结论银杏叶提取物在大鼠脑再灌注损伤中可通过保持抑制性氨基酸/兴奋性氨基酸、自由基系统的平衡及快速抑制谷氨酸诱导大鼠海马神经元内游离钙浓度升高来保护受损的神经元的.
目的研究銀杏葉提取物(GBE)對大鼠缺血再灌註損傷皮質內自由基、氨基痠動態平衡的影響及其對原代培養的大鼠海馬神經元內遊離鈣離子濃度([Ca2+]i)的影響和特徵.方法採用的動物模型參照Zivin JV 的大腦中動脈線栓模型以穫得缺血/再灌註損傷的皮質組織樣本.採用高壓液相色譜儀測量氨基痠的濃度;MDA和GSH-PX採用TBA法測量,SOD採用嘌呤法測量.使用顯微熒光檢測繫統檢測單箇原代培養的海馬神經元內遊離鈣離子濃度([Ca2+]i)的變化和特徵.結果和對照組比較,治療組中,SOD和GSH-PX 的濃度較高, MDA的濃度則明顯降低, 穀氨痠、天門鼕氨痠的濃度明顯降低,而GABA的濃度在各箇時間點均升高(P<0.01), Gly的濃度在一些時間點有所降低 (P<0.05), 5 mg/kg 組與10 mg/kg、15 mg/kg組間有顯著差彆,而後二者間差彆無顯著意義.噹嚮原代培養的神經元同時給予1×10-5 mol/L穀氨痠和25 μg/mlGBE20秒時所誘導的[Ca2+]i明顯低于單獨使用1×10-5 mol/L穀氨痠所引起的[Ca2+]I的變化,其峰值明顯下降,且Phase 1上升速度減慢,Phase 2的時間也有所縮短,二相之間的平檯期相對延長,噹其返迴基線後,再次給予1×10-5 mol/L穀氨痠時,其反應可恢複.結論銀杏葉提取物在大鼠腦再灌註損傷中可通過保持抑製性氨基痠/興奮性氨基痠、自由基繫統的平衡及快速抑製穀氨痠誘導大鼠海馬神經元內遊離鈣濃度升高來保護受損的神經元的.
목적연구은행협제취물(GBE)대대서결혈재관주손상피질내자유기、안기산동태평형적영향급기대원대배양적대서해마신경원내유리개리자농도([Ca2+]i)적영향화특정.방법채용적동물모형삼조Zivin JV 적대뇌중동맥선전모형이획득결혈/재관주손상적피질조직양본.채용고압액상색보의측량안기산적농도;MDA화GSH-PX채용TBA법측량,SOD채용표령법측량.사용현미형광검측계통검측단개원대배양적해마신경원내유리개리자농도([Ca2+]i)적변화화특정.결과화대조조비교,치료조중,SOD화GSH-PX 적농도교고, MDA적농도칙명현강저, 곡안산、천문동안산적농도명현강저,이GABA적농도재각개시간점균승고(P<0.01), Gly적농도재일사시간점유소강저 (P<0.05), 5 mg/kg 조여10 mg/kg、15 mg/kg조간유현저차별,이후이자간차별무현저의의.당향원대배양적신경원동시급여1×10-5 mol/L곡안산화25 μg/mlGBE20초시소유도적[Ca2+]i명현저우단독사용1×10-5 mol/L곡안산소인기적[Ca2+]I적변화,기봉치명현하강,차Phase 1상승속도감만,Phase 2적시간야유소축단,이상지간적평태기상대연장,당기반회기선후,재차급여1×10-5 mol/L곡안산시,기반응가회복.결론은행협제취물재대서뇌재관주손상중가통과보지억제성안기산/흥강성안기산、자유기계통적평형급쾌속억제곡안산유도대서해마신경원내유리개농도승고래보호수손적신경원적.
Objective To study the effect of Ginkgo biloba extract on rats during ischemia/reperfusion and its influence on intracellular calcium in hippocampal neurons. Methods Model of intraluminal occlusion of the middle cerebral artery (MCAO) was used to prepare the ischemia/reperfusion cortex tissue. Concentration of MDA was determined by measuring thiobarbituric acid-reactive substance. GSH-PX was quantified using the thiobarbituric acid (TBA) technique. SOD was assayed througha xanthine method. Endogenous amino acids were quantified by high performance liquid chromatographic (HPLC) analysis. Primary culturs of hippocampal neurons were prepared for a free intracellular calcium ([Ca2+]I ) assay by Fura-2 based single cell microfluoremetric technique.Results Comparing control and treatment groups, the concentration of SOD and GSH-PX were higher, whereas that of MDA was much lower; the concentration of glutamate and aspartate decreased and that of GABA increased markedly at all time point (P<0.01), Gly also decreased at some time points (P<0.05). The differences were significant between the groups of 10 mg/kg, 15 mg/kg and the groups of 5 mg/kg. When 1×10-5 mol/L glutamate was applied with 25 μg/ml ginkgo biloba extract to cultured neurons, the increase in [Ca2+]I was lower than that caused by applying glutamate alone. Its peak value was much lower and increased phase was longer, its declining phase was shorter. After returning to baseline, the application of 1×10-5 mol/L glutamate could induce the reaction to recover.Conclusions Ginkgo biloba extract could protect damaged neurons by keeping the balance of inhibitory/excitatory aminoacids, enhancing the free radical scavengers system, and inhibiting the effect of glutamate on [Ca2+]I.